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Human Endothelium: Target for Aldosterone
Hans Oberleithner, Thomas Ludwig, Christoph Riethmüller, Uta Hillebrand, Lars Albermann, Claudia Schäfer, Victor Shahin, Hermann Schillers
+ Author Affiliations

From the Institute of Physiology II, Nanolab, University Münster, Germany.
Correspondence to Dr Hans Oberleithner, Institut für Physiologie, Robert-Koch-Str 27a, 48149 Münster, Germany. E-mail oberlei@uni-muenster.de
Abstract

Aldosterone has long been known to control water and electrolyte balance by acting on mineralocorticoid receptors in kidney. However, recent studies demonstrated the presence of these receptors in nonclassical locations, including the cardiovascular system. We tested the hypothesis whether endothelial cells respond to aldosterone with changes in cell volume, a measure for ion-mediated water movement across the cell membrane. By means of atomic force microscopy in fluid, we measured volume of adherent human umbilical venous endothelial cells exposed for 72 hours to 10 nmol/L aldosterone. Over this period of time, cells swell by ≈18%. Aldosterone-induced swelling is prevented by 100 nmol/L of the mineralocorticoid receptor antagonist spironolactone, added to the primary endothelial cell culture. Aldosterone-treated cells dramatically shrink when 1 μmol/L of the diuretic amiloride is applied. Cells deprived of aldosterone do not respond to amiloride. Our conclusions are: (1) aldosterone leads to sustained cell swelling inhibited by administration of spironolactone or the sodium channel blocker amiloride; (2) cells respond to amiloride after aldosterone exposure; (3) renal diuretics act on endothelial cells; and (4) both amiloride and spironolactone could be useful for medical applications to prevent aldosterone-mediated endothelial dysfunction.